Switch from protective to adverse inflammation during influenza: viral determinants and hemostasis are caught as culprits

• Published in: Cellular and molecular life sciences : CMLS Vol. 71; no. 5; pp. 885 - 898
• Main Authors: Berri, Fatma, Lê, Vuong Ba, Jandrot-Perrus, Martine, Lina, Bruno, Riteau, Béatrice
• Format: Journal Article
• Language: English
• Published: Basel Springer-Verlag 01.03.2014; Springer Basel; Springer Nature B.V; Springer Verlag
• Subjects: Biochemistry; Biomedical and Life Sciences; Biomedicine; Cell Biology; hemostasis; Hemostasis - immunology; HLA-G Antigens - metabolism; Homeostasis; Humans; Immune response; Immunity, Innate - immunology; Immunologic Surveillance - immunology; inflammation; Inflammation - etiology; Inflammation - immunology; Inflammatory diseases; Influenza; Influenza, Human - immunology; innate immunity; Life Sciences; lungs; Models, Immunological; Orthomyxoviridae; pandemic; Pandemics; Receptor, PAR-1 - metabolism; Review; Viral Nonstructural Proteins - metabolism; Viral Proteins - metabolism; viruses; Influenza virus; Hemostasis; PAR1; Inflammation; Plasminogen; Innate immune sensors; Fibrinolysis; HLA-G; NATURAL-KILLER-CELLS; HLA-G EXPRESSION; INNATE IMMUNE-RESPONSE; ACUTE LUNG INJURY; RIG-I; VIRUS NS1 PROTEIN; CYTOTOXIC T-LYMPHOCYTES; A VIRUS; PLASMINOGEN DEFICIENCY; ENDOTHELIAL-CELLS
• ISSN: 1420-682X; 1420-9071
• DOI: 10.1007/s00018-013-1479-x

Influenza viruses cause acute respiratory infections, which are highly contagious and occur as seasonal epidemic and sporadic pandemic outbreaks. Innate immune response is activated shortly after infection with influenza A viruses (IAV), affording effective protection of the host. However, this response should be tightly regulated, as insufficient inflammation may result in virus escape from immunosurveillance. In contrast, excessive inflammation may result in bystander lung tissue damage, loss of respiratory capacity, and deterioration of the clinical outcome of IAV infections. In this review, we give a comprehensive overview of the innate immune response to IAV infection and summarize the most important findings on how the host can inappropriately respond to influenza.